ArticleFrontiers in oncology2023
PFDN2 promotes cell cycle progression via the hnRNPD-MYBL2 axis in gastric cancer.
Article in Frontiers in oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- RNA-binding protein hnRNPD induces epithelial-mesenchymal transition in Wilms' tumor via facilitating MAP4K4 mRNA stability.Molecular genetics and genomics : MGG · 2026Article
- PFDN2 stabilizes PYCR2 to activate Wnt/β-catenin signaling and promote colorectal cancer progression.Scientific reports · 2026Article
- Integrative analysis of RiboSis-related gene expression in colorectal cancer: implications for prognosis and immunotherapy.Apoptosis : an international journal on programmed cell death · 2025Article
- A novel 5'tRNA-derived fragment tRF-Tyr inhibits tumor progression by targeting hnRNPD in gastric cancer.Cell communication and signaling : CCS · 2025Article
- PFDN4 as a Prognostic Marker Was Associated with Chemotherapy Resistance through CREBP1/AURKA Pathway in Triple-Negative Breast Cancer.International journal of molecular sciences · 2024Article
- Establishment and Validation of Novel Prognostic Subtypes in Hepatocellular Carcinoma Based on Bile Acid Metabolism Gene Signatures Using Bulk and Single-Cell RNA-Seq Data.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastric cancer (GC) is a major health burden worldwide, but our understanding of GC is limited, and the prognosis is poor. Novel therapeutic strategies and biomarkers are urgently needed to improve GC patient outcomes. Previously, we identified PFDN2 as a novel key gene in gastric cancer based on its differential expression between cancer and normal tissues. However, the role and underlying mechanisms of PFDN2 in GC remain elusive. In this article, we demonstrated that PFDN2 is highly expressed in GC and that upregulation of PFDN2 is associated with the progression of GC. We further found that PFDN2 could promote cell cycle progression by promoting MYBL2 expression. Mechanistically, we demonstrated that PFDN2 could upregulate MYBL2 expression by facilitating the nuclear translocation of hnRNPD, and thus promoting MYBL2 transcriptional program. In conclusion, we found that PFDN2 promotes cell cycle progression via the hnRNPD-MYBL2 axis and may serve as a potential biomarker and therapeutic target for GC.
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Registered trials
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